Multiple Sclerosis
Introduction
Autoimmune nervous system disorders include multiple sclerosis, myasthenia gravis and Guillain-Barre syndrome.
Multiple sclerosis :
an immune-mediated progressive demelinating disease fo the CNS
The fatty and protein material, myelin is destroyed in the brain and spinal cord
Result : impaired transmission of nerve impulses
Incidence
In young adults 20 - 40
Women > men
Aetiology
Auto immune activity results in demyelination
Sensitized antigen has not been identified
Multiple factors play a role in initiation of the immune process
A genetic predisposition is indicated by the presence of a specific cluster (haplotype) of human leukocyte antigens (HLA) on the cell wall
These antigens may promote susceptibility to factors such as viruses
DNA on the virus mimics the amino acide sequence of myelin
Pathophysiology
Sensitized T cells cross the blood-brain barrier
The T cells promote the infiltration of agents that damage the immune system and leads to inflammation of the myelin and destruction of the myelin and the oligodendroglial cells that produce myelin.
Plaques of sclerotic tissue appear on demelinated axons, interrupting the transmission of impulses
Demyelinated axons are scattered irregularly throughout the CNS.
Most affected areas are : optic nerves, chiasm, tracts, cerebrum, the brain stem, cerebellum and spinal cord
Eventually axons themselves degenerate resluting in permanent and irreversible damage
Clinical Manifestations
The course may be benign with a normal life span with such mild symptoms that the patients never seek treatment
Remissions and exacerbations +
Quadriparesis
Cognitive dysfunction
Visual loss / visual disturbances / blurring of vision / diplopia / patchy blindness (scotoma)
Brain stem syndromes
Fatigue
Depression
Weakness
Numbness
Difficulty in co-ordination
Loss of balance
Pain
Suicidal tendencies
Spacity of the extremities / loss of abdominal reflexes (Pyramidal tract)
Sensory dysfunction -- paresthesias, pain
Frontal and parietal lobe involvement → memory loss, decreased concentration (Cognitive changes)
Involvement of cerebellum or basal ganglia → ataxia and tremor
Emotional lability and euphoria
Bladder, bowel and sexual dysfunctions
Secondarily urinary tract infections, constipation, pressure ulcers, contracture deformities, dpendent pedal edema, pneumonia, reactive depression, decreased bone mass
Investigations
MRI - visualize plaques
Electrophoresis of CSF - oligoclonal banding (several bands of immunoglobulin G bonded together
Evoked potential studies - extent of the disease process and monitor changes
Urodynamic studies - to assess the bladder dysfunction
Neuropshychological testing - to assess cognitive impairment
Medical Management
No cure
An individualized, organized and rational treatment program to be evolved
Pharmacologic Therapy
ABC (and R) drugs
Interferons beta - 1a (Avonex)
Beta-1b (Betaseron
Glatiramer acetate (Copaxone)
Rebif
All these have multiple immune activities
Itoxantrone (Novantrone) to treat secondary progressive MS
Corticosteroids
Baclofen (Lioresal) for spasms
Benzodiazepines (Valium), tizanidine and dantrolene (dantrium) for spasms
